Variant human breast tumor estrogen receptor with constitutive transcriptional activity

Journal Article

Since progesterone receptor (PgR) is normally induced by estrogen, breast cancers lacking estrogen receptor (ER) would also be expected to lack PgR. However, a small percentage of breast cancers are ER- yet PgR+. These tumors might possess an ER which is defective in estrogen binding but is still functional in stimulating estrogen-responsive genes such as PgR. We have now detected such a variant, lacking exon 5 of the hormone-binding domain, using complementary DNA amplified by the polymerase chain reaction. This variant was the predominate ER RNA expressed in three ER-/PgR+ tumors. Furthermore, the variant ER constitutively activates transcription of a normally estrogen-dependent gene construct in yeast cells. The variant ER could explain the expression of PgR in certain tumors and have therapeutic implications.

Duke Authors

Cited Authors

  • Fuqua, SAW; Fitzgerald, SD; Chamness, GC; Tandon, AK; McDonnell, DP; Nawaz, Z; O'Malley, BW; McGuire, WL

Published Date

  • 1991

Published In

Volume / Issue

  • 51 / 1

Start / End Page

  • 105 - 109

International Standard Serial Number (ISSN)

  • 0008-5472